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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the effect of vasogenic brain edema on the brainstem, the relationships between waveform changes in brainstem auditory evoked potentials (BAEP) and blood-brain barrier (BBB) disturbance following transient hindbrain ischemia were investigated. Hindbrain ischemia was induced in gerbils by bilateral occlusion of the vertebral arteries. The animals were divided into three groups subjected to 0, 5, and 30 min of bilateral vertebral occlusion (BVO-0',-5', and -30' groups; n = 4 in each group). Two hours after recirculation, Evans blue (EB) solution was injected into the saphenous vein. The brains were removed after 30 min of circulation, and all areas stained macroscopically by EB were noted and recorded. During hindbrain ischemia, BAEP disappeared within 3 min. In the BVO-5' group, BAEP reappeared and returned to normal within 10 min after reperfusion, whereas in the BVO-30' group, BAEP never returned to normal and finally disappeared within 30 min after reperfusion. In the BVO-5' group, no EB staining was visible. On the other hand, in the BVO-30' group, EB staining was seen in the medial part of the tegmentum in the midbrain in two animals, and around the vestibular nucleus in the lateral parts of the pons in three. These results demonstrate the close relationship between the reversibility of ischemia-induced changes in BAEP and BBB disturbance in the brainstem.
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PMID:An ischemic opening of the blood-brain barrier may deteriorate brain stem auditory evoked potentials following transient hindbrain ischemia in gerbils. 797 44

Cerebral edema is one of the major consequences of head trauma (HT); its evolution may cause secondary ischemia and neuronal damage. In a closed head injury model in rats, we have shown BBB disruption and edema formation during the post traumatic period. We have previously shown that chronic exposure to moderate heat improves clinical outcome of rats subjected to HT. Long term exposure to heat results in the achievement of a stable acclimated state, characterized by a lower metabolic rate and improved heat tolerance. In the present study, we investigated the effect of chronic exposure to heat on edema formation after HT. Rats were held at 24 degrees C (CON) or 34 degrees C (ACC) for one month. Injury was then induced under ether anesthesia by a weight drop device. Four or 48 hours later, they were sacrificed for evaluation of BBB integrity (Evans blue, EB, extravasation) or edema formation (specific gravity, SG, or percent water). We found that EB uptake by the contused hemisphere was 6 fold lower in the ACC rats as compared to CON (p < 0.001). Furthermore, edema measured at 48 h by both SG and percent water methods was significantly lower in the acclimated rats (p < 0.01). We suggest that heat acclimation offers protection to rats subjected to head injury, possibly by reduction of plasma proteins extravasation.
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PMID:Long term exposure to heat reduces edema formation after closed head injury in the rat. 797 14

Mild to moderate hypothermia (30-33 degrees C) reduces brain injury after brief (< 2-h) periods of focal ischemia, but its effectiveness in prolonged temporary ischemia is not fully understood. Thirty-two Sprague-Dawley rats anesthetized with 1.5% isoflurane underwent 3 h of middle cerebral artery occlusion under hypothermic (33 degrees C) or normothermic (37 degrees C) conditions followed by 3 or 21 h of reperfusion under normothermic conditions (n = 8/group). Laser-Doppler estimates of cortical blood flow showed that intraischemic hypothermia reduced both postischemic hyperperfusion (p < or = 0.01) and postischemic delayed hypoperfusion (p < or = 0.01). Hypothermia reduced the extent of blood-brain barrier (BBB) disruption as estimated from the extravasation of Evans blue dye at 6 h after the onset of ischemia (p < or = 0.01). Hypothermia also reduced the volume of both brain edema (p < or = 0.01) and neuronal damage (p < or = 0.01) as estimated from Nissl-stained slides at both 6 and 24 h after the onset of ischemia. These results demonstrate that mild intraischemic hypothermia reduces tissue injury after prolonged temporary ischemia, possibly by attenuating postischemic blood flow disturbances and by reducing vasogenic edema resulting from BBB disruption.
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PMID:Mild intraischemic hypothermia reduces postischemic hyperperfusion, delayed postischemic hypoperfusion, blood-brain barrier disruption, brain edema, and neuronal damage volume after temporary focal cerebral ischemia in rats. 801 9

At the present time there is no final explanation for the etiology of Bell's palsy. The theory of pathophysiology involving a combined primary and/or secondary ischemia is now well-accepted. As such, it is supposed that there is a dysfunction of the blood vessels which supply the nerve. This is followed by a hyperpermeability and transudation which lead to edema of the nerve and compression of the blood supply. The vicious circle starts and the final result is facial paralysis. The blood supply of the facial nerve has been described previously in the literature, although there have been no experimental investigations on in vivo perfusion of the nerve. In the present study we evaluated the percentage of those vessels perfused among the total blood vessels found in facial nerves of Wistar rats. Animals were examined after i.v.-injections of Evans blue dye, with perfused vessels demonstrable under a fluorescence microscope. Forty-eight hours later, the same tissue section was stained by indirect immunofluorescence and the primary antibody used was directed against myosin of non-muscle sources. This antibody cross-reacted with myosin of vascular endothelial cells and thus allowed identification of any existing blood vessels. More than 90% of the immunostained vessels were labeled with the dye, showing that almost all vessels were perfused.
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PMID:[Blood supply to the facial nerve]. 802 Nov 58

Leukocytes, in particular polymorphonuclear neutrophils (PMNs), are believed to play a central role in ischemia-reperfusion (I/R)-induced tissue injury. Changes in endothelial cells occurring during ischemia promote PMN binding to these cells during reperfusion, which primers PMN synthesis of oxygen radicals and release of cytotoxic proteins. These events lead to vascular damage and subsequent tissue injury. Recently we have shown that doxycycline (Dc), a member of the tetracycline family of antibiotics, inhibits PMN superoxide (O2) synthesis and degranulation in vitro. It also suppresses PMN-mediated RBC, fibroblast, and endothelial cytotoxicity, properties of the drug that may make it of use to protect tissues from I/R-induced injury. In this study we demonstrate that Dc administration either prior to clamping of the portal circulation, or 1 h after the reperfusion, significantly suppressed liver damage as assessed by serum levels of a marker of hepatic injury, alanine aminotransferase (s-ALT). The reduction in s-ALT was not a result of reduced reflow in the Dc-treated rats as indicated by Evans' blue perfusion data. The findings suggest that Dc and possibly other tetracyclines may be of value in protecting tissues and organs from I/R-mediated damage even if the drug is given after the ischemic event has occurred.
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PMID:Doxycycline suppression of ischemia-reperfusion-induced hepatic injury. 807 Sep 3

Although fibroblast growth factor has been identified in normal and ischemic myocardium, temporal changes in mitogenic activity due to fibroblast growth factors in ischemic tissue have not been well established, nor has correlation been made with the known early increases in coronary collateral flow. This study sought to measure fibroblast growth factor activity in myocardium after coronary ligation. Accordingly the left anterior descending coronary artery of dogs was ligated and coronary collateral flow measured with radioactive microspheres. The heart was arrested after 2 h (four dogs), 1 week (four dogs), 2 weeks (three dogs), or 8 weeks (four dogs). Just before arrest collateral flow was again measured with radioactive microspheres, and the perfusion territory of the ligated vessel was demarcated with an intracoronary injection of Evans blue. The stained ischemic region was separated into central and peripheral portions. A transmural sample was removed from each portion for quantitation of tissue radioactivity and the rest was used for isolation of fibroblast growth factor and the measurement of mitogenic activity with vascular endothelial cells. To determine which fibroblast growth factor (FGF-1 or FGF-2) was being produced by the myocardium, aliquots of the isolated protein were first treated with specific antibodies to FGF-1 or FGF-2 before being assayed for mitogenicity. Coronary collateral flow did not change between 5 min and 2 h following coronary ligation, but was significantly increased at later time points. The ischemic/normal myocardial basic fibroblast growth factor mitogenic activity ratio in the peripheral ischemic tissue was increased after 2 h of ischemia (1.41 +/- 0.34), but the increase was not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal changes in myocardial basic fibroblast growth factor (FGF-2) activity following coronary artery ligation in the dog. 807 23

Basic fibroblast growth factor is a polypeptide with potent multipotential trophic effects on central nervous system cells, including neurons, glia, and endothelial cells. In particular, it promotes the survival of a wide variety of brain neurons in vitro, and protects these neurons against the effects of several neurotoxins, including excitatory amino acids, hypoglycemia, and calcium ionophore. Since lack of substrate delivery, excitatory amino acid toxicity, and calcium entry into cells appear to be important processes in neuronal death after ischemia, we tested the hypothesis that pretreatment with basic fibroblast growth factor limits infarct size in a model of focal cerebral ischemia in vivo. Mature male Long-Evans rats received either continuous intraventricular infusion of basic fibroblast growth factor (1.2 micrograms/day; with or without heparin, added to stabilize the growth factor) or vehicle alone for 3 days before focal ischemic infarcts were made in the right lateral cerebral cortex by permanent distal middle cerebral artery occlusion and temporary (45-minute) bilateral carotid occlusion. Intraoperative measurements of core temperature, arterial blood pressure and blood gases, blood glucose concentration, and hematocrit, and postoperative measurements of temperature revealed no differences among vehicle- versus basic fibroblast growth factor-treated animals. Twenty-four hours later, animals were killed, brains were removed and stained to visualize cortical infarcts, and infarct volume was determined by image analysis. Overall, we found a 25% reduction in infarct volume in basic fibroblast growth factor- (N = 25) versus vehicle-treated (N = 23) animals (p < 0.01). This reduction was not enhanced by the addition of heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pretreatment with intraventricular basic fibroblast growth factor decreases infarct size following focal cerebral ischemia in rats. 815 72

Blood-brain barrier permeability alteration, vasogenic brain edema, and infarction, which are more extensive after 3 hours of temporary middle cerebral artery occlusion (MCAO) and 3 hours of reperfusion than after 6 hours of permanent MCAO, develop in rats after prolonged focal cerebral ischemia. Protective effects of excitatory amino acid receptor antagonists have been previously demonstrated after temporary global ischemia and permanent focal ischemia in rats. The purpose of this study was to evaluate the effectiveness of MK-801, a noncompetitive N-methyl-D-aspartate receptor antagonist, in temporary middle cerebral artery occlusion in rats maintained at physiological levels of brain temperature. Rats were anesthetized with chloral hydrate (350 mg/kg, intraperitoneally). The MCAO of rats was occluded by cannulation with a nylon suture for 3 hours, followed by 3 hours of reperfusion accomplished by withdrawing the suture. MK-801 (1 mg/kg, intravenously) or saline (S) was injected immediately before the onset of MCAO. Water content (MK-801, n = 6; S, n = 6), Evans blue dye extravasation (MK-801, n = 6; S, n = 6), infarct volume (MK-801, n = 10; S, n = 10), histology (MK-801, n = 6; S, n = 6), and neurological deficit (MK-801, n = 15; S, n = 18) were measured at the end of 3 hours of reperfusion. Brain temperature was monitored during the experiment. The infarction area (measured by 2, 3, 5-triphenyltetrazolium chloride staining) was reduced (P < 0.001) in the MK-801-treated rats, as was the infarct volume and the severity of neuronal damage (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of vasogenic edema and infarction by MK-801 in rats after temporary focal cerebral ischemia. 817 96

Brain polyamines have been associated with posttraumatic vasogenic edema and blood-brain barrier (BBB) breakdown seen in some models of brain injury. We hypothesized that the inhibition of the enzyme responsible for polyamine production with the decarboxylase difluoromethylornithine (DFMO) may decrease BBB breakdown after a focal brain ischemic stroke. Thirty-two cats underwent 8 hours of middle cerebral artery occlusion and one of four treatments: sham operation (Sham), ischemia (Isc), ischemia/DFMO (Isc/DF), and ischemia/DFMO/putrescine (Isc/DF/PU). The regional brain specific gravity and the volume of Evans blue (EB) extravasation were measured at the time of death. The groups were monitored for temperature, heart rate, blood pressure, and arterial blood gases, and the values did not differ outside normal physiological ranges. EB results were expressed as the percentage of the hemisphere stained and showed the following: Sham, 2.23%; Isc, 32.8%; Isc/DF, 5.6%; Isc/DF/PU, 36.3%. As a measure of BBB, ischemia increased EB staining; DFMO pretreatment decreased the amount of EB staining to control levels; and the polyamine putrescine abolished the protective effect of DFMO (all significant at P = 0.05). DFMO pretreatment also resulted in a significant (P = 0.05) return to control values for specific gravity in the EB-stained regions (1.0328) of ischemic animals. This effect was present primarily in the white matter. Treatment with DFMO, an ornithine decarboxylase inhibitor, significantly decreased postischemic BBB breakdown and vasogenic edema in this model.
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PMID:Difluoromethylornithine decreases postischemic brain edema and blood-brain barrier breakdown. 826 88

Gut ischemia/reperfusion (I/R) appears to produce pulmonary vascular injury through endotoxin release and cytokine activation. The ability of hepatic reticuloendothelial cells to clear bacterial products may also be impaired during I/R. To test this, diversion of the splanchnic blood flow from the liver into the systemic circulation was performed via a microsurgical portacaval transposition in anesthetized Sprague-Dawley rats (275-375 g). Shunted animals underwent portacaval transposition and were allowed to recover for 7-10 days; sham animals underwent exploration but no shunt was created. The I/R animals were subjected to 60 minutes of reperfusion. All shunts were patent at autopsy. Pulmonary vascular permeability was assessed by measuring tissue retention of Evans blue dye. Gut I/R produced significant increases in pulmonary vascular permeability (46.2% +/- 11.0% vs. 16.4% +/- 3.8% [I/R vs. control]; p < 0.05) regardless of the presence of hepatic bypass (32.7% +/- 9.0% vs. 10.0% +/- 1.4% [I/R vs. control]; p < 0.05). These data indicate that a mediator or mediators of gut origin are responsible for pulmonary vascular permeability changes following gut I/R and are not appreciably modulated by the liver.
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PMID:Lung injury from gut ischemia: insensitivity to portal blood flow diversion. 841 Dec 71


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